Periodontitis (or periodontal disease) is an inflammatory disease of the supporting tissues of the teeth. Disease progression is characterized by formation of a periodontal pocket (harbouring bacterial plaque), progressive destruction of supporting connective tissue and loss of alveolar bone, leading to progressive loosening and eventual loss of teeth. Periodontal disease is associated with specific bacteria in subgingival dental plaque. Porphyromonas gingivalis is considered one of the most etiologically important pathogens associated with periodontitis and its progression. This black-pigmented, asaccharolytic, Gram-negative anaerobe, relies on the metabolism of specific amino acids for energy. P. gingivalis has an absolute requirement for iron, preferentially in the form of heme or its Fe(III) oxidation product hemin and when grown under conditions of excess hemin is highly virulent in experimental animals.
A number of virulence factors have been implicated in the pathogenicity of P. gingivalis including the capsule, adhesins, cytotoxins and extracellular hydrolytic enzymes. A major virulence factor and vaccine candidate of the P. gingivalis are the extracellular cysteine proteinases or gingipains (RgpA, RgpB and Kgp). These have been extensively studied (1-8). The gingipain complex alone has been shown to protect against periodontal bone loss in prophylactic animal models and antibodies specific to this complex have demonstrated protective efficacy in human studies (9,10). Despite this, virulence and the disease-causing capacity of P. gingivalis may likely be multifactoral, involving a number of determinants (11).
The genome of P. gingivalis strains W83 and ATCC 33277 have each been sequenced (12,13), but these references do not provide any teaching on which P. gingivalis antigens are immunogenic and otherwise useful.
Consequently, there remains a need for effective treatments of P. gingivalis infections.